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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sleep disturbances in psychoses can mean hypo- as well as hypersomnia. In 90% of endogenous depressed patients sleep disturbances were seen, mostly as hyposomnia. In the group of schizophrenic psychotic patients only 30% had sleep disturbances. With polygraphical investigations in endogenous depressed patients a shortening of REM-latency and a disturbed sleep profile, in schizophrenic psychoses a shortened REM-rebound and a reduced amount of stages 3 and 4 were found. The treatment of choice for depressions are antidepressive drugs and sleep deprivation, for schizophrenic psychoses neuroleptic drugs. This treatments improved subjective and objective sleep disturbances with psychopathological remission at the same time. So far, only hypothetical considerations do exist about the relationship between psychopathology and sleep disturbances. It is suspected that etiological relations exist between depression and desynchronization of central sleep mechanisms and between schizophrenia and special disturbances of REM-sleep and stage 3 and 4.
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PMID:[Sleep problems and their treatment in psychosis (author's transl)]. 4 23

The efficacy of psychopharmacological treatment modalities and comatose methods was studied in the therapy of patients with slowly progressive schizophrenia, the clinical picture of which was characterized by cenestho-hypochondriacal disturbances (155 cases). The use of high doses of neuroleptics, atropine and insulin comas in these cases were ineffective. A positive compliance to therapy was attained in the treatment by tranquilizers of the benzodiazepine series, especially by a parenteral administration. The best results were demonstrated in the treatment of pseudoneurotic hypochondria. The therapeutic reluctancy increased in the cenestho-algic syndrome and in the syndrome of "rigid" hypochondria. The most effective in these cases was a combined therapy by tranquilizers (parenteral administration) and small doses of neuroleptics.
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PMID:[Psychopharmacotherapy of slowly progressive hypochondriacal schizophrenia]. 4 44

The steady rise in the promiscuous use of phencyclidine (PCP) as a "recreational" drug has recently gained nationwide attention because of the numerous violent and/or bizarre incidents caused by the use of this drug. Because the media often exaggerate reports of bizarre and violent behavior to make a "good" story, the potential PCP user may be tempted to ignore the media warnings. In the case of PCP, however exaggerated the story, a real danger does exist. So, despite numerous newspaper, radio and television warnings about the possible consequences of PCP use and abuse, the incidence of toxic reactions continues to climb. In many cases PCP is sold as other drugs, particularly THC, and in various colored capsules, tablets, liquids and crystals which may explain the increased usage despite the numerous warnings against its use. The advances in laboratory techniques and chemical processess have enabled the clandestine chemist to prepare relatively pure PCP and thus eliminate many of the toxic side effects due to impurities in the drug. In addition, 30 or more psychoactive PCP analogues have been developed and are starting to make an appearance on the street. PCP is perhaps the most potent psychotomimetic compound known at the present time and is capable of inducing a psychosis which is clinically indistinguishable from schizophrenia. The psychosis-producing effects of PCP are the most common toxic effects seen in hospital emergency rooms; but as the amount of PCP taken and/or the simultaneous involvement of other drugs, particularly barbiturates, occurs, severe medical problems (e.g., coma, seizures, respiratory arrest) begin to appear. Death from high doses of PCP or PCP plus other drugs does occur, but the principal cause of death from PCP abuse is due to trauma, homicide or suicide (usually of the bizarre or violent form). Young adult males, persons predisposed to mental illness and naive drug users appear to be the most susceptible to the adverse effects of PCP. The fact that chronic PCP users are starting to increase in number is mute testimony that not all users experience "bad trips" with PCP. Unfortunately for the user, however, this does not guarantee that the next trip will not be a bad one. The effects of chronic use seem to be twofold: severe depression with suicidal thoughts and numerous violent, agitated behavioral patterns. Neither seems to be a suitable alternative. At the present time there is not specific antidote for toxic PCP reactions and the prolonged psychosis induced in some cases does not appear to respond to the standard antipsychotic medications as quickly as do the functional psychoses. The major improvement from a medical standpoint is the development of more sensitive laboratory techniques to confirm the presence of PCP in body fluids. This advance has undoubtedly led to the apparent increase in the number of PCP cases reported by hospitals and to the accuracy of clinical diagnosis by medical, drug or law enforcement communities...
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PMID:PCP (phencyclidine): an update. 4 8

The amine theory of affective disorder and the dopamine and endorphin theories of schizophrenia are controversial but heuristically valuable concepts that have emerged from the psychobiological revolution of the last decade. That revolution stemmed largely from the development of techniques for localizing and assaying neuroregulators and their receptors in the brain under normal, pathological and experimental conditions. The data thus obtained are reviewed here, and the current status of the emergent psychobiological hypotheses assessed.
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PMID:Brain amines and peptides--their relevance to psychiatry. 4 87

The effects of the antipsychotic/antidepressant drug CI-686 on apomorphine- and amphetamine-induced stereotypies, dopamine metabolism, neuroleptic binding, and serum prolactin levels were determined. CI-686 displayed profiles of activity in each of these systems that differs markedly from those of other antipsychotics. CI-686's unique preclinical profile suggests a mechanism of action other than dopamine antagonism which could have implications regarding current thinking on the pathophysiology of schizophrenia.
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PMID:Atypical antidopaminergic properties of CI-686: a potential antipsychotic agent. 4 73

This is a retrospective study of 100 child-patients with schizophrenia seen in the Child Psychiatric Clinic over a period of 4 years. Some personal and family characteristics of this group of patients are presented. Their clinical features, management and outcome are also presented and discussed.
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PMID:A clinical profile of 100 child-patients with schizophrenia. 4 26

The diagnosis of schizophrenia is established principally by the presence of certain psychological symptoms which although subjective can be reliably assessed by standardized interviewing procedures. The most characteristic symptoms (Schneider's first-rank symptoms) fall into three groups: (a) auditory hallucinations of particular types, (b) 'ego-boundary disturbances', including intrusions into the stream of consciousness attributed to external agencies, and (c) delusional perception. Symptoms closely resembling those seen in schizophrenia can be induced in non-schizophrenic individuals by amphetamine-like drugs, and both these symptoms and those of schizophrenia are ameliorated by neuroleptic drugs (the major tranquillizers). Amphetamines facilitate and neuroleptic drugs diminish neural transmission mediated by the chemical substance dopamine. In recent post-mortem studies on patients who had suffered brom schizophrenia, it was found that dopamine release was not increased. However, in some cases there was evidence of increased sensitivity of the dopamine receptor.
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PMID:Schizophrenia: the nature of the psychological disturbance and its possible neurochemcial basis. 4 59

The organisation of the central nervous system (CNS) is considered from the point of view of the chemical specificity of neurons with respect to their neurotransmitters. The mechanisms of neurotransmission are summarized as well as the approaches used to determine the neurotransmitters of specific CNS pathways. As an example, the neurotransmitters of the basal ganglion and their interactions are presented and their implications for the pathophysiology of Huntington disease and possibly schizophrenia are discussed.
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PMID:[Central organization of transmitter systems]. 4 40

Metabolic theories of manic-depressive psychosis and schizophrenia are reviewed and constructivist models are presented which attempt to integrate biochemical, neurophysiological and clinical findings.
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PMID:[Physiopathology of endogenous psychoses]. 4 42

Several pieces of evidence support the view that GABA neurons inhibit the DA system both in extrapyramidal and limbic regions. This inhibition is exerted on cell bodies and terminals of DA neurons and is involved in the regulation of their activity. A recently synthesized GABAmimetic compound SL 76.002 has considerably helped in elucidating the role of GABA in this regulation as well as the therapeutic implication of changes of GABAergic transmission in human brain. Thus, impairment of dopaminergic transmission by SL 76.002 has been shown to be effective in iatrogenic extrapyramidal syndromes such as L-DOPA-induced involuntary movements in parkinsonian patients and neuroleptic-induced tardive dyskinesias: the first attributed to an exaggerated formation and liberation of DA, the second to supersensitivity of target cells of DA neurons. Furthermore, GABAergic medication has been confirmed to be useful in Huntington's chorea in which some symptoms originate from degeneration of striatal GABAergic neurons. Finally, GABAergic inhibition on cellular excitability has been proved to ameliorate epilepsy. However, SL 76.002, contrary to the expectation, was not effective in schizophrenia suggesting that GABA does not play a major role in the pathogenesis of this disorder.
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PMID:[Potential therapeutic activity of GABA-mimetic drugs in neuropsychiatry]. 4 43


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